Total radioactive residues and clenbuterol residues in edible tissues, and the stereochemical composition of clenbuterol in livers of broilers after exposure to three levels of dietary [14C]clenbuterol HCl and three preslaughter withdrawal periods.

Thirty-six broiler chickens were randomly assigned to .5, 1.0, or 2.0 ppm dietary [14C]clenbuterol HCl for a 2-wk period starting at 5 wk of age. Four birds from each treatment were slaughtered after withdrawal periods of 0, 7, or 14 d. Total radioactive residues (TRR; clenbuterol HCl equivalents) were measured in adipose tissue, kidney, liver, skin with adhering adipose tissue, bile, blood, brain, gastrointestinal tract, heart, lung, spleen, and testes; parent clenbuterol was measured in liver and kidney. In edible tissues, TRR were roughly proportional to dietary [14C]clenbuterol level and inversely proportional to duration of the withdrawal period; kidney TRR ranged from nondetectable (14 d of withdrawal, .5 and 1.0 ppm treatments) to 211.5 ppb for the 2.0 ppm treatment at zero withdrawal. Liver TRR were detectable for all treatment and withdrawal periods. Rapid depletion of TRR from edible tissues occurred during the first 7 d of the withdrawal period, but depletion of TRR was much slower thereafter. Parent clenbuterol was below the limit of detection (1 ppb) or was undetectable in liver and kidney for all dietary levels after 7 and 14 d of withdrawal, but it represented 22 to 48% of the total radioactive residues at 0 withdrawal. The inactive S (+) stereoisomer constituted approximately 73% of the total clenbuterol residue in livers of chickens slaughtered with no withdrawal period, and the active R (-) stereoisomer accounted for the remainder. These data indicate that radioactive residues of clenbuterol were present well after parent clenbuterol had depleted from edible tissues in chickens, and the predominant stereoisomer remaining in livers at slaughter was the inactive isomer.